Prevention is managed through proper sanitation and good hygiene.

Enterobius vermicularis:

General characteristics:

 Enterobius vermicularis (pinworm) is distributed worldwide and commonly identified in group settings of

children ages 5 to 10 years. The life cycle is considered direct; transmission occurs from an infected host to

another individual , During the night, the mature female worm migrates out of the anus of the infected host and

lays eggs in the perianal region. The embryonated eggs will mature and a third-stage larva stage develops,

resulting in infectivity within hours. Transmission occurs by ingestion or inhalation of eggs. Reinfection may also

occur when the eggs hatch and larvae return to the intestine where they mature.

Epidemiology:

 Pinworm is more prevalent in school-age children up to about 14 years of age. Infections are associated with

institutional crowding and are familial. Transmission is also associated with an increased rate of reinfection

within agroup or autoinfection from hatched larvae.

Pathogenesis and spectrum of disease:

 Infections with E. vermicularis are typically asymptomatic. The most common complaint is perianal pruritus

(itching) and resultant restless sleep. Occasionally, the parasite may migrate to other nearby tissues, causing

pelvic, cervical, or peritoneal granulomas.

Laboratory diagnosis:

Diagnosis is typically by microscopic identification of the characteristic flat-sided ovum (Figure 33).

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The eggs are collected using a sticky paddle or cellophane tape pressed against the perianal region. Eggs are not

typically identified in feces, although they may occasionally

be found in a stool specimen. Although adult pinworms may be visible, they can be easily confused with small

pieces of thread. The female worm measures 8 to 13 mm long with a pointed “pin” shaped tail. In gravid

females, almost the entire body will be filled with eggs (Figure 34). The males measure only 2 to 5 mm in

length, die following fertilization, and may be passed in feces.

Therapy:

Anthelmintic therapy is generally effective with one of the following agents: albendazole, mebendazole,

pyrantel pamoate, or ivermectin.

Prevention:

Regular good personal hygiene is the major factor for prevention of continued reinfection and autoinfection.

Strongyloides stercoralis:

General characteristics:

 Infection with Strongyloides stercoralis is less common than other intestinal nematodes.

S. stercoralis, commonly referred to as the threadworm, may inhabit the intestine or exist as a free-living

organism in the soil. The life cycle can be classified as direct, indirect (free-living phase), or autoinfective ,The

filariform (infective larvae) penetrate the skin and migrate via the circulatory system to the heart and lungs.

The organism enters the bronchial tree and then is swallowed, where it lives in the digestive tract and matures

into an adult worm. In the intestine the filariform larvae may also penetrate the mucosa, resulting in

autoinfection.

The female worm produces eggs by parthenogenesis (a form of asexual reproduction where growth and

development occur without fertilization), because parasitic adult male worms are nonexistent. Within the

indirectlife cycle, the rhabditiform (noninfective) larvae develop into mature males and egg-producing females

(Figure 35).

Figure 33: Enterobius vermicularis eggs Figure 34: Enterobius vermicularis gravid female.

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Epidemiology:

 S. stercoralis is transmitted via direct penetration in endemic areas. Person-to-person transmission occurs

within institutionalized groups, in day care centers, and among homosexual men.

Pathogenesis and spectrum of disease:

Infections may be asymptomatic or consist of a variety of disseminated strongyloidiasis syndromes.

Reinfection is more commonly associated with immunocompromised patients. Acute infections may develop a

localized pruritic, erythematous papular rash. Some patients develop a macropapular or urticarial (red and

raised) rash on the buttocks, perineum, and thighs. The migration of larvae may cause epigastric pain, nausea,

diarrhea, and blood loss. Hyperinfection, an increased worm burden within the lungs and intestines, may occur.

Disseminated infections may also result in larvae within the central nervous system, kidneys, and liver.

A second species, Strongyloides fuelleborni, a primate parasite, has been isolated from humans in Africa and

causes a severe life-threatening condition called “swollen belly syndrome.”

Laboratory diagnosis:

The rhabditiform larva is the primary diagnostic stage for strongyloidiasis in humans through microscopic

examination of stool. The larvae are 250 to 300 μm long with

a short buccal capsule, a large bulb on the esophagus, and a prominent genital primordium ,The filariform

larvae are larger (up to 500 μm) and have a notched tail with an esophageal to intestinal ratio of 1 : 1.

The eggs, which are rarely identified, are segmented with a thin shell. S. stercoralis larvae are the most

common found in human stool specimens.

 Although not available in routine laboratories, realtime polymerase chain reaction (PCR) methods have been

developed that amplify the small subunit of the rRNA gene. The assay is used to detect DNA in fecal samples

and has a demonstrated sensitivity and specificity of 100%. A high throughput multiplex assay has also been

developed that includes primer and probe pairs for S. stercoralis as well as other intestinal nematodes and

protozoa.

Figure 35 Strongyloides stercoralis rhabditiform larva, iodine stain

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Additional specimens such as sputum, body fluids, and tissues may be used for the diagnosis of

hyperinfections.

Therapy:

Ivermectin is the recommended treatment for uncomplicated infections. Albendazole is an alternative.

Prevention:

Immunocompromised individuals and patients taking immunosuppressive medications should avoid

contaminated beaches and other areas.

Trichostrongylus spp.:

General characteristics:

 Although commonly found in mammals and birds worldwide, approximately 10 different species of

Trichostrongylus have been found in human infections. The worms are small and live in the mucosa of the

small intestine. The adult worm has no visible buccal capsule.

Pathogenesis and spectrum of disease:

Following ingestion of the larvae, the larvae mature and migrate through the lungs. Symptoms are related to

the worm burden and the amount of damage within the intestine.

Laboratory diagnosis:

 Laboratory diagnosis includes identification of eggs or hatched larvae in the stool. The eggs are oval and

resemble hookworm eggs except they are slightly longer and more pointed (Figure 36). Larvae should be

differentiated from hookworm and S. stercoralis .

Therapy:

Anthelmintic agents are recommended including mebendazole and pyrantel pamoate. Albendazole is the

treatment of choice.

Figure 36 Trichostrongylus sp. egg.

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Prevention:

 Thorough washing of plant material, including cultivated vegetables, before handling or ingestion is

recommended.

Trichuris trichiura:

General characteristics:

 Trichuris trichiura, whipworm, has a worldwide distribution. Unlike other intestinal nematodes there is no

tissue migration phase within the life cycle of T. trichiura.

Epidemiology:

 Humans are infected by ingestion of the eggs. Larvae are released in the intestine ,where they mature into

adult worms. Eggs are then passed in the feces and deposited in the soil. The eggs require a warm, moist

environment for embryonation in order to become infective to another host.

Pathogenesis and spectrum of disease:

Pathogenesis and severity of the disease are closely related to the worm burden. The lack of symptoms is

related to the life cycle that does not include a tissue migration stage, as is seen in other nematode

infections.Infections range from mild, very low worm burden, to severe infections with bleeding and weight

loss in heavy worm infestations. The characteristic whiplike worm buries its threadlike anterior into the

intestinal mucosa and feeds on tissue secretions, causing an inflammatory reaction and peripheral eosinophilia.

Laboratory diagnosis:

 Diagnosis is typically from the identification of eggs and rarely the adult worm within the feces.

(Figure37,38).

Therapy:

Anthelmintics such as albendazole are recommended when necessary.

Figure 37 Trichuris trichiura egg. Note the clearly evident

polar hyaline plugs.

Figure 38 Adult female Trichuris trichiura.

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Prevention:

 Prevention includes practicing proper hygiene and sanitation as well as the disposal of dirt or soil

contaminated with feces.

Capillaria philippinensis:

General characteristics:

 Human infection is thought to occur from the ingestion of uncooked fish harboring infective larvae. The

people ingest a large spectrum of raw seafood, including fish, shrimp, crabs, and snails.

Pathogenesis and spectrum of disease

Symptoms vary with the level of worm burden. The larvae are ingested and reside in the small intestine where

they burrow into the mucosa. Because of the mechanical insertion into the intestinal wall, patients lose weight

rapidly as a result of malabsorption and fluid loss. Long term infections lasting weeks to months may result in

death attributable to a severe loss of electrolytes, particularly potassium (hypokalemia), and associated organ

Laboratory diagnosis:

 Diagnosis is typically from the identification of eggs, adult worms, or larvae in stool specimens. The eggs

resemble those produced by T. trichiura. They are somewhat smaller with a thick, striated shell and less

prominent polar plugs. Female worms produce the characteristic thick-shelled eggs as well as thin-shelled and

free larvae.

Therapy

Anthelmintic agents including albendazole and mebendazole are recommended.

Prevention

Adequate preparation and cooking of seafood, including fish, snails, crabs, and shrimp in endemic areas, are

encouraged.

Hookworms:

 Hookworms are known to have a worldwide distribution with two species known to infect humans,

Ancylostoma duodenale (Figure 39) and Necator americanus . They are the second most common helmintic

infection reported in humans. The eggs and rhabditi- form larvae of the two species are indistinguishable.

Differentiation of the species is based on the morphology of the buccal capsule and the adult male copulatory

bursa (see Figure 40)

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.

The parasites, infective filariform larvae, penetrate the skin and enter the circulation where the larvae are

capable of breaking through the capillaries and entering the lungs of the host. The larvae migrate up the

bronchial tree, over the epiglottis, and are swallowed. Upon entering the digestive system, the hookworms

attach to the mucosa of the small intestine. Here they secrete anticoagulants and ingest blood as their source of

nourishment.

The worms mature and eggs are passed in the feces and deposited in soil where they mature into rhabditiform

larvae. The noninfective rhabditiform larvae will then mature into filariform.

Ancylostoma duodenale:

General characteristics

 The adult male tends to be larger than the adult male of N. americanus. They attach to the intestinal mucosa by

well-developed mouthparts, especially teeth (see Figure 39).

Pathogenesis and spectrum of disease :

A. duodenale is capable of maturation within the intestine without migrating through the lungs of the host.

Necator americanus:

General characteristics

N. americanus, New World hookworm, attach to the intestinal mucosa by well-developed cutting plates (see

Figure 40).

Figure 39: A, Ancylostoma duodenale head. B, Tail; note the appearance of the pointed tail

 Figure 40 A, Necator americanus head; note the clearly evident rounded cutting plates protruding from the head. B,

Copulatory bursa.

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Pathogenesis and spectrum of disease

 Skin-associated symptoms as described for hookworms Eosinophilia peaks in approximately 2 months in

gastrointestinal phase.

Laboratory diagnosis

 Hookworms are typically diagnosed by the presence of eggs or rhabditiform larvae found in stool specimens.

The eggs and larvae of the two species are indistinguishable.

The eggs are oval and thin-shelled and contain a clearly visible four- to eight-cell stage embryo. There is a characteristic

clear space between the shell and the developing embryo (see figure 40). Recovery and identification of eggs on direct smear

or from concentration methods is recommended. Eggs may appear distorted on permanently stained smears. The

rhabditiform larvae are typically 250 to 300 μm with a long buccal capsule and an inconspicuous genital primoridum

(Figures 41 and 42). The larger filariform larvae are approximately 500 μm, with a pointed tail and a esophageal to intestinal

ratio of 1 : 4. Both the rhabditiform and filariform larvae must be differentiated from S. stercoralis.

Fresh stool stored at room temperature may result in continued maturation and hatching of larvae.

Therapy:

Anthelmintic agents including albendazole, mebendazole, and pyrantel pamoate are indicated.

Prevention

Avoid contaminated soil and beaches. Wear appropriate footwear such as enclosed shoes in potentially contaminated areas.

Tissue Nematodes (Roundworms):

Figure 41: Hookworm egg, iodine stain. Figure 42 Hookworm rhabditiform larvae.

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Helminths Nematodes (Roundworms) Tissue:

Trichinella spiralis

Visceral larva migrans (Toxocara canis or Toxocara cati)

Ocular larva migrans (Toxocara canis or Toxocara cati)

Cutaneous larva migrans (Ancylostoma braziliense or Ancylostoma

caninum)

Dracunculus medinensis

Parastrongylus (Angiostrongylus) cantonensis

Parastrongylus (Angiostrongylus) costaricensis

Gnathostoma spinigerum

 Tissue nematodes have life cycles similar to those of intestinal nematodes, consisting of five distinct stages

including adult male and female worms and four larval stages. These organisms are distributed worldwide,

predominantly in the tropics and subtropics. The organisms are transmitted by three routes: biting and

subsequent blood-feeding arthropods (filarial worms), ingestion of small freshwater crustaceans; and ingestion

of contaminated meat. In most cases, adult worms do not multiply and develop within the human host. Clinical

symptoms are dependent on the number of infecting parasites, the tissue invaded, and the host’s general health

and immune response. Diagnosis is typically by th microscopic visualization of the organisms in tissue when

appropriate.

Trichinella spiralis:

General characteristics:

The family Trichinellidae contains 11 recognized species including Trichinella spiralis, Trichinella nativa,

Trichinella nelsoni, T. murrelli, T. papuae, T. zimbabwensis, T. pseudospiralis, and T. britovi, all capable of

causing trichinosis.

However, T. spiralis is the most common human pathogen. The organism is unique in comparison to other

helminths in that all stages of development, including the adult and larval stages, occur within a single host.

Epidemiology

Trichinella occurs worldwide with the cycle maintained in several different mammalian species. The mammal

serves as the definitive host for the adult worm and the intermediate host for the encysted larvae. Humans

acquire the infection by eating undercooked meat that contains the infective encysted larvae. Although this is

typically transmitted in pork, human cases have been associated with ingestion of bear, walrus, horsemeat, and

other mammals.

The encysted larvae are ingested. When the undercooked meat is digested in the stomach, the larvae are

resistant to the gastric pH and pass to the intestine, where they invade the mucosa. In about 1.5 days, the larvae

mature and mate, and the female worm begins to

release motile larvae. These larvae then migrate to the lymphatic system or mesenteric venules and become

distributed throughout the body. The larvae then deposit

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in the striated muscle tissue, where they can continue development, coil, and encyst, becoming infective. The

larvae encyst in the active striated muscle including the

diaphragm, larynx, tongue, jaws, neck, ribs, biceps, and gastrocnemius.. The larvae may remain viable within

the cyst for several years. The larvae eventually die and the

encysted capsules become calcified.

Pathogenesis and spectrum of disease

Trichinosis is a disease of the muscle caused by infection with the encysted larval form of Trichinella spp.

(Figure 43). The adult stages reside in the human intestine.

The disease ranges from mild to severe dependent on the number of parasites present. The intestinal stage lasts

approximately 1 week and typically includes mild symptoms of nausea, abdominal discomfort, diarrhea, and/or

constipation. Diarrhea may last as long as 14 weeks with no apparent muscle involvement. The migration of the

larvae results in an intense inflammatory response causing periorbital edema, fever, muscle pain or

tenderness, headache, and myalgia. A marked peripheral eosinophilia is often present. If the parasitic infection

is low, eosinophilia may be the only diagnostic sign evident.

Occasionally, splinter hemorrhages may be present below the nails.

In addition to the typical infection of the active striated muscle as previously indicated, occasionally larvae will

migrate into the brain, meninges, and myocardium.

However, the larvae will not encyst in these tissues. Brain and meningeal infections will result in neurologic

symptoms, and infection of the myocardium may result in myocarditis and dysrhythmias leading to sudden

death.

Laboratory diagnosis :

 Diagnosis may be difficult, because the symptoms may resemble a variety of flulike illnesses. A thorough

patient history is required to assist the physician in diagnosing the condition in a timely fashion. Identification

of encysted larvae through muscle biopsy provides definitive diagnosis. However, based on location, some

Figure 43: Trichinosis. Encysted larvae within tissue.

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tissues may be difficult to access and therefore the condition may not be diagnosed until the postmortem

examination.

Histologic examination of formalin-fixed or paraffin-imbedded tissue may be used to visualize encysted larvae.

Occasionally, dependent on the length of infection, calcified larvae may be seen in x-rays.

Serologic diagnosis is sufficient in most cases. Patients will present with a specific antibody response in 3 to 5

weeks following acute illness. A negative serologic test followed by a positive seroconversion is considered

definitive diagnosis.

Molecular species–specific polymerase chain reaction (PCR) has been developed.

Therapy :

 Thiabendazole is used during the intestinal phase to reduce the number of potentially infective larvae, and

although the encysted larvae cannot be removed, albendazole

is used to limit the continued pathologic development of the organism. Supportive measures including

analgesics and steroids may be administered to lessen the effects of the generalized inflammatory response.

Prevention

Most effective prevention relies on eating only thoroughly cooked meat as well as maintaining good animal

husbandry for domestic swine.

TOXOCARA CANIS (VISCERAL LARVA MIGRANS) AND TOXOCARA CATI (OCULAR LARVA

MIGRANS):

General characteristics

 Toxocara canis (intestinal ascarid of dogs) and Toxocara cati (intestinal ascarid of cats) are the cause of a

human syndrome resulting from larval migration within the host.

Epidemiology

Toxocariasis is a zoonotic disease with worldwide distribution. Humans become infected with the accidental

ingestion of eggs (Figure 44). The definitive hosts, dogs (T. canis) and cats (T. cati), pass the larvae

transplacentally or lactogenically to their offspring and pass unembryonated eggs in the feces. The eggs mature

in 10 to 20 days, and then become infective. Once the eggs are ingested, the larvae are released in the small

intestine penetrate the mucosa, and migrate to the liver, lungs, or other body sites. The larvae migrate up the

respiratory tract and are swallowed, returning to the intestinal tract where they mature into adult worms. The

adult worms are unable to mature in a human host and therefore wander throughout the body causing the

migratory syndromes.

Pathogenesis and spectrum of disease

Typically the infections are mild but may be severe. Severe life-threatening infections occur when there is

involvement in the heart, brain, or other vital organs.

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Disease is frequently found in young children and may persist for long periods with minimal pathologic

manifestations. Larvae that remain in the liver or lungs may become encapsulated in fibrous tissue. Visceral

(tissue) larva migrans (VLM) may result in a high degree of eosinophilia; however, this may be absent in ocular

larva migrans (OLM). Symptoms may include fever, hepatomegaly, hyperglobulinemia, pulmonary infiltration,

cough, neurologic symptoms, and endophthalmitis.

OLM may result in the development of a granulomatous reaction in the retina of the eye.

Laboratory diagnosis

Toxocariasis must be differentiated from other migratory helmintic diseases including A. lumbricoides, S.

stercoralis, and Trichinella spp. A history of exposure to dogs and cats

is of importance when considering an infection with Toxocara spp. Because humans are an insufficient host for

completion of the organism’s life cycle, eggs are not passed in the stool. Diagnosis typically requires biopsy of

tissue.

Serologic diagnosis has proven effective, particularly in OLM. Aqueous humor–elevated antibody titer specific

for Toxocara spp., in comparison to serum levels, is considered diagnostic. Although serologic testing has been

useful, it is important to note that antibody titers may vary depending on the location of the infection. A serum

titer of 1 : 8 is considered significant for OLM; 1 : 32 is significant for VLM.

Therapy

Effective therapy depends on the location of infection but several anthelmintic medications have been used

including thiabendazole, ivermectin, albendazole, and diethylcarbamazine.

Prevention

Small children should be kept out of sandboxes and playgrounds frequented by dogs and cats. In addition,

regular deworming of dogs and cat will reduce the spread of infective eggs.

 Figure 44: Toxocara canis egg. Note the rough appearance on the outer

surface of the egg. The egg also contains an infectious L2 larvae.

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Ancylostoma braziliense or ancylostoma caninum (cutaneous larva migrans):

General characteristics

Ancylostoma braziliense and Anycylostoma caninum are common hookworms of dogs and cats. The parasites

penetrate the skin and cause cutaneous larva migrans (CLM), also referred to as creeping eruption.

Epidemiology

The organisms are found in warm climates within the Southeastern United States. Dogs and cats are the natural

definitive host for Ancylostoma spp. The infective larvae penetrate the skin of the host and migrate in the

circulation. The adult worms reside in the intestine. The eggs are shed in the feces of dogs and cats. The eggs

undergo maturation in moist, sandy soil in areas protected from desiccation, such as under shady trees and

houses. Children are often infected when playing in sandboxes that have been contaminated with dog and cat

feces.

Pathogenesis and spectrum of disease

The infective larvae penetrate the skin of the human host and migrate through the subcutaneous tissue. The host

develops pruritic papules at the site of penetration, followed

by serpiginous, vesicular, elevated linear tracks. The larvae will migrate severa millimeters each day, forming

these continued tracks. The area surrounding the tracks becomes inflamed with marked edema.

The patient may present with a peripheral eosinophilia. Infection is typically self-limiting. As the larvae

migrate, the host may scratch and scar the tissue, subjecting the host to potential secondary bacterial infections.

The signs and symptoms resemble those of infection with similar insect larvae, Strongyloides stercoralis, and

other animal hookworms.

Systemic involvement is rare; however, cases of pneumonitis resulting from larvae migration into the lungs

have been identified. In addition, gastrointestinal discomfort including abdominal pain, diarrhea, and weight

loss has been associated with Ancylostoma spp. infections. This condition is referred to as eosinophilic enteritis.

Laboratory diagnosis

Laboratory diagnosis is limited. Evidence of visible tracks and patient history of possible exposure are usually

sufficient. The patient may present with a peripheral eosinophilia. In systemic cases, larvae may be recovered

from sputum and Charcot-Leyden crystals may be evident.

Therapy

Anthelmintic therapy may include ivermectin or thiabendazole.

Dracunculus medinensis:

General characteristics

Dracunculus medinensis, commonly referred to as the guinea worm, is the cause of a subcutaneous infection

known as dracunculiasis. The worm has a characteristic, thick cuticle and a large uterus that fills the body

cavity and contains rhabditoid larvae.

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Epidemiology

Humans are infected by the ingestion of freshwater from stagnant ponds containing larvae-infected copepods.

The copepods are digested in the stomach, releasing the larvae. The larvae penetrate the small intestine and

migrate through the thoracic musculature. Both adult male and female worms mature in approximately 2 to 3

months. The gravid female develops in approximately 10 to 14 months, migrating to the lower extremities. The

gravid female produces a blister on the skin, and when the host submerges the affected area in water, the blister

erupts and releases larvae into the water.

Pathogenesis and spectrum of disease

The blisters formed by the gravid female worm cause burning and itching. Systemic symptoms may include

fever, nausea, vomiting, diarrhea, headache, urticarial and eosinophilia. Secondary bacterial infections may

occur. In addition, dead worms within the host may be absorbed or may calcify, causing secondary

inflammatory symptoms.

Laboratory diagnosis

Diagnosis is by identification of larvae or adult worms.

Therapy

Treatment requires removal of the adult worms. The female worms are attached to a stick and slowly retracted

from the host by gradual turning of the stick and remova of the worm. Although anthelmintic medications,

such as metronidazole or thiabendazole, are not lethal, they are administered to assist with the retraction of the

worms. Analgesics and antimicrobials are administered for discomfort and the prevention of secondary

infections.

Parastrongylus cantonensis

(Cerebral angiostrongyliasis):

General characteristics

Parastrongylus cantonensis, previously known as Angiostrongylus sp., is a filiarial worm commonly referred to

as the rat lungworm.